Dealing With ACOG 163 and the Importance of Neuroimaging
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Presented by E. Drew Britcher, Esq. of Britcher Leone, LLC
For any Plaintiff’s attorney prosecuting birth injury cases dealing with the publications of the American College of Obstetricians and Gynecologists (ACOG) is essential. ACOG’s publications can either become a great resource for proving the standard of care or they can be the death of your case.
The most common publication that a plaintiff’s attorney in a medical malpractice case must deal with is ACOG Technical Bulletin 163, first published in 1992. ACOG Technical Bulletin 163 claims to set forth the criteria for determining whether a fetus allegedly suffered asphyxia during the delivery process resulting in brain damage. The criteria set forth in ACOG Technical Bulletin 163, were later incorporated into ACOG Committee Opinion 137, published in 1994, and ACOG Committee Opinion 197, published in 1998. These publications set forth four criteria that ACOG claims must be established before a “plausible link” can be made between a defendant’s negligence resulting in perinatal asphyxia and neurologic injury can be proven. These are:
Profound metabolic or mixed acidemia found in the infant’s umbilical cord arterial blood, exhibited by a pH of less than 7.00;
APGAR scores of a newborn child persistently from 0-3 for more than five minutes;
Subsequent medical documentation of neonatal neurological sequelae, illustrated by seizures, hypotonia or coma; and
Dysfunction exhibited in any or all of the newborn child’s cardiovascular, gastrointestinal, hematologic, pulmonary or renal systems.
While most plaintiff’s attorneys agree that ACOG 163, and the other publications have been to help obstetricians defend medical malpractice lawsuits, juries can still be swayed by such an important sounding group having codified these standards. Thus, plaintiff’s attorney’s must look at the variety of available attacks on ACOG 163 and alternative means of proving causation.
There are several articles or publications that should be known by any Plaintiff’s attorney seeking to deal with the ACOG 163 criteria . These include, but are not limited to Dr. Goodlin’s article published in the American Journal of Obstetrics and Gynecology in June of 1995 entitled, “Do concept’s of Causes of Prevention of Cerebral Palsy Require Revision”, Dr. Korst’s articles published in Prenatal Neonatal Medicine in 1997 and in the Journal of Maternal Fetal Medicine in a 1997, the latter being entitled, “Acute Fetal Asphyxia and Permanent Brain Injury, a Retrospective Analysis of Current Indicators”, the International Cerebral Palsy Task Force statement published in the British Medical Journal in 1999 entitled “A Template for defining a Causal Relation Between Acute Intrapartum Events and Cerebral Palsy: International Consensus Statement”, Dr. Volpe’s textbook, “Neurology of the Newborn” 4th Edition, published in 2001, “The Continuing Value of the Apgar Score for the Assessment of Newborn Infants”, published in the New England Journal of Medicine in 2001 and the Report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society, published as a Practice Parameter: Neuroimaging of the Neonate in June 2002.
The Goodlin article was one of the first peer-reviewed publications to call in to question the criteria established by ACOG 163. Dr. Goodlin reviewed four cases of intrapartum fetal insults with subsequent cerebral palsy, all of which were considered to demonstrate the link between the two, but all of which lacked the necessary criteria under ACOG 163 to qualify. His ultimate conclusion was that exceptions to the criteria exist and that despite the appeal to obstetricians to apply these criteria as hard and fast rules, a revisiting of the criteria was needed. As noted in his article, one can question whether the purpose of the criteria was to be too limiting, as “when they are applied, few cases of cerebral palsy appear to be due to perinatal asphyxia.”
In the first of the Korst articles a similar review of 16 severely neurologically impaired term infants was undertaken. All of these had been subject to an acute intrapartum event, such as uterine rupture or prolapsing of the cord. Each had been diagnosed as suffering from hypoxic-ischemic encephalopathy and had no other identified cause of their brain injury, However, when the ACOG 163 criteria were applied only one of the 16 met all 4 criteria, 4 met 3 of the criteria, 8 met 2 criteria and 3 met only 1 criteria. The following were the specific findings for each criteria:
- Five had a pH <7.00
- Five had a 5 minute Apgar score <3
- 13 had seizures within the first 24 hours
- 8 had no multiorgan dysfunction, while 4 had 1 system dysfunction and 4 had more than 1.
In the second study they reported on 47 neonates of similar condition. Their findings were:
- 10 met all 4 criteria
- 14 met 3 criteria
- 14 met 2 criteria
- 8 met 1 criterion
- 1 met no criteria
Also they found:
- the mean pH was 7.06, with only 38percent <7.00
- 26 had a five minute Apgar <3
- 87 percent experienced seizures within the first 24 hours
- 70 percent had multi-organ dysfunction
Their conclusion was “Our retrospective study suggests that currently used indicators to define permanent fetal brain injury are not valid.”
The International Consensus provides the following criteria, differing from ACOG 163. It should be noted that the American College of Obstetricians and Gynecologists are listed as supporters of this statement:
1. Evidence of a metabolic acidosis in intrapartum fetal, umbilical cord or very early neonatal blood samples, pH<7 and base deficit > -12 mmol/L
2. Early onset of severe of moderate neonatal encephalopathy in infants > 34 weeks gestation
3. Cerebral Palsy is of the spastic quadriplegic or dyskinetic type.
Criteria that together suggest an intrapartum timing, but by themselves are non specific.
4. A sentinel event occurring immediately before or during labour
5. A sudden, rapid and sustained deterioration of the fetal heart rate pattern usually following the sentinel event where the pattern was previously normal.
6. Apgar scores of 0-6 for longer than 5 minutes
7. Early evidence of multi-system involvement.
8. Early imaging evidence of acute cerebral abnormality.
Dr. Volpe’s textbook (both the 3rd and 4th Editions) carries a very useful Tables that can be used effectively to undermine the 163 criteria. Table 9-3 in the 3rd Edition shows that 34% of asphyxiated infants have no organ injury and the 4th Edition in the same table has 22%.The New England Journal article examines the history of the Apgar score and discusses its proper purpose and it’s misuse for determining long term neurological outcome. While finding that ‘the Apgar scoring system remains as relevant for the prediction of neonatal survival today as it was almost 50 years ago” the authors conclude with ” We cannot dispute the contemporary viewpoint that the use of the Apgar score for the prediction of long-term neurologic outcome is inappropriate. However, the poor performance of the Apgar system as a predictor of neurologic development, a purpose for which it was never intended…….” Clearly this article provides a valuable argument in a case where the subjective Apgar scores are inconsistent with the child’s condition at birth and beyond.
The Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society in the Practice Parameter published in 2002 provide the following useful information. Neuroimaging plays two important roles: 1) diagnosis of brain injury in the newborn at risk so that appropriate medical management can be provided and 2) detection of those lesions associated with long-term neurodevelopmental disability. Currently, cranial ultrasonography (US), CT, and MRI are the most available means for these tasks.
Clinical examination of the term infant with signs and symptoms of neonatal encephalopathy is often unable to determine the severity or extent of cerebral damage and frequently provides little information regarding the etiology of the insult. Although numerous reports suggest that hypoxic-ischemic encephalopathy (HIE) is a common cause of neonatal encephalopathy, the differential diagnosis of this condition is extensive, including a spectrum of abnormalities ranging from infectious to metabolic abnormalities and congenital malformations. Even in those infants with documented HIE, the clinical presentation may vary widely. Of those neonates with moderate to severe HIE, almost one-quarter have mental retardation, seizures, and CP, and promising intervention strategies are now becoming available. Therefore, for diagnostic and prognostic reasons, early assessment and diagnosis of infants with neonatal encephalopathy is important.